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Counterpulsation in dogs with normal systemic arterial blood pressure produced a reduction in myocardial oxygen consumption without a significant concomitant change in total coronary flow. In dogs with a deteriorating heart and low systemic arterial blood pressure, myocardial oxygen consumption became dependent on coronary flow. Under these circumstances, counterpulsation produced an increase in coronary flow, and with it a secondary augmentation of cardiac oxygen consumption. Counterpulsation reduced the mean systemic arterial blood pressure during ventricular ejection to a greater degree when the control level of this pressure was normal than when it was hypotensive. This lessened effect may also occur when the heart has deteriorated. The mechanisms involved in causing the several effects of counterpulsation are discussed. ADDITIONAL KEY WORDSaortic blood flow and pressure pulses right heart by-pass left ventricular pressure and work dp/dt mean ejection pressure phasic coronary flow pump effect cardiac oxygen consumption alteration in pump phasing dogs• The use of assisted circulation has been proposed for a variety of conditions which produce circulatory collapse, e.g., hemorrhagic, cardiogenic and septicemic shock. There are three possible methods which may support the heart under such circumstances: (1) to put a pump in series with the heart, (2) to place a pump in parallel with the heart or to by-pass one of the ventricles, and (3) to replace the heart with an artificial one. We are concerned with a pump in series with the heart. Harken's group (1) introduced the concept of counterpulsation by placing a reciprocating This work was supported by Grant N65-12 from the Chicago Heart Association and by Grant HE-0&375 from the National Institutes of Health, U. S. Public Health Service.Dr. Hirsch was an Advanced Research Fellow of the American Heart Association.Dr. Lluch is a Postdoctoral Research Fellow supported by departmental Training Crant HTS-5252 from the National Heart Institute, U. S. Public Health Service.Accepted for publication October 3, 1966. pump in series with the heart. The way counterpulsation supports the heart can be briefly stated. The pump is synchronized with the electrocardiogram (ECG) so that the pump removes blood from the aorta during ventricular systole, reducing the afterload against which the heart contracts and thereby the cardiac work load. During ventricular diastole, the pump returns the blood to the aorta under pressure, thereby raising the diastolic pressure in the aorta, and in this way, presumably also providing a greater flow of blood through the coronary arteries during this phase of the cycle. Since this is the phase during which most of the coronary flow occurs, it should lead, all other things being equal, to an increase in over-all coronary flow. Jacobey et al. (2, 3) observed an increased collateral circulation in the hearts of animals which had been treated by counterpulsation. However, since they did not present quantitative data, it is difficult to evalua...

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Fifteen untrained, unanesthetized dogs were infused intravenously with blood for 10 min at the rate of 100 ml/min. The heart rate changes so induced were compared with the heart rate existing initially. Systemic arterial and venous pressures were also recorded by means of indwelling catheters. The direction of change in heart rate was found to depend on the initial heart rate. When the initial heart rate was below 120 beats/min the infusion caused a tachycardia; above this initial rate a bradycardia was induced. Denervation was carried out in 26 other dogs. Sympathectomy and "total" denervation of the heart tended to abolish the induced tachycardia, but not the induced bradycardia. Vagotomy did not abolish the induced bradycardia. In ten vagotomized dogs the initial rate was above 120 beats/min.

An animal model of cardiogenic shock has been developed in the intact unanesthetized dog. Selective embolization of the circumflex coronary artery with 0.2 ml of mercury produces infarction of the posterolateral wall of the left ventricle and a shocklike state in the dog which results in death of the animal in 5 to 48 hr. The syndrome of cardiogenic shock in the animal model simulates closely that observed in man. Systemic blood pressure falls sharply (25 to 30% of control) immediately after embolization, remains low for several hours, then slowly increases toward normal, but never reaches preinfarct levels. The left ventricular end-diastolic pressure (LVEDP) remains within normal limits (5 to 10 mm Hg) during the initial hypotensive state, but increases to values above 10 mm Hg during the period of rising systemic pressures. As left ventricular failure begins to develop as evidenced by the rise in LVEDP, the mean pulmonary artery pressure also rises above control values. The cardiac output falls to 40% of control levels following embolization and never recovers. Peripheral resistance rises to compensate for the reduction of cardiac output and remains above control levels. Electrocardiograms indicate an essentially normal sinus rhythm with short runs (5 to 15 beats) of ventricular tachycardia with A-V dissociation. The hypotensive state does not seem to be related to this arrhythmia. Death of the animal appears to be due to progressive failure of the left ventricular pump to maintain cardiac output and systemic pressures.

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